A pathogen is any organism or agent that can cause disease. The DSE specification requires knowledge of four main types of pathogen.
Pathogen Type Structure Examples of Diseases Key Features Bacteria Prokaryotic cells; no nucleus; cell wall (peptidoglycan); single circular chromosome; 70S ribosomes; plasmids Cholera, tuberculosis, gonorrhoea, tetanus, syphilis Reproduce by binary fission (rapid, every 20 min); produce toxins (endotoxins and exotoxins); most are free-living; treated with antibiotics Viruses Non-cellular; protein coat (capsid) surrounding nucleic acid (DNA or RNA); no ribosomes; no metabolism; no cell membrane Influenza, HIV/AIDS, COVID-19, measles, polio, HPV Obligate intracellular parasites; replicate inside host cells using host machinery; not affected by antibiotics Fungi Eukaryotic; chitin cell wall; true nucleus; 80S ribosomes; can be unicellular (yeasts) or multicellular (moulds) Athlete”s foot, ringworm, thrush (Candida) Reproduce by spores; saprotrophic nutrition; treated with antifungal drugs Protozoa Eukaryotic; unicellular; no cell wall; true nucleus; some have flagella or cilia Malaria (Plasmodium), amoebic dysentery, sleeping sickness Often have complex life cycles involving multiple hosts; transmitted by vectors (e.g., mosquitoes for malaria)
Pathogens cause disease through several mechanisms:
1. Production of toxins:
Toxin Type Description Example Exotoxins Secreted by living bacteria into the surrounding environment; highly potent; specific targets (nerves, cells, etc.) Tetanus toxin (Clostridium tetani); cholera toxin (Vibrio cholerae) Endotoxins Components of the outer membrane of Gram-negative bacteria; released when bacteria die; less potent but cause fever and inflammation Lipopolysaccharide (LPS) from Salmonella, E. Coli
2. Cell damage:
Viruses replicate inside host cells, causing cell lysis and tissue damage Some bacteria produce enzymes that damage host tissues (e.g., hyaluronidase, which breaks down connective tissue, facilitating spread) Protozoa such as Plasmodium destroy red blood cells during their life cycle 3. Host immune response:
The symptoms of many diseases (fever, inflammation, tissue damage) are caused by the body’s own immune response, not directly by the pathogen For example, the severe lung damage in severe influenza is largely caused by an overactive immune response (cytokine storm) Transmission Route Description Example Direct contact Physical contact with an infected person (skin, bodily fluids) Herpes simplex, HIV, HPV Droplet infection Coughing, sneezing, talking expels droplets containing pathogens Influenza, common cold, COVID-19, tuberculosis Water-borne Ingestion of contaminated water Cholera, typhoid, amoebic dysentery Food-borne Ingestion of contaminated food (undercooked meat, unwashed vegetables) Salmonella, E. Coli O157, botulism Vector-borne Transmission by an insect or other animal vector Malaria (mosquito), dengue fever (mosquito), Lyme disease (tick) Fomite transmission Transfer via contaminated objects (door handles, towels, medical equipment) Common cold viruses, MRSA Blood-borne Transfer through blood or blood products HIV, Hepatitis B and C
The body’s first line of defence prevents pathogens from entering the body.
Barrier Mechanism Skin Physical barrier; keratinised outer layer (epidermis) is tough and water…/1-number-and-algebra/3_proof-and-logic; sebaceous glands secrete sebum (antimicrobial lipids) Mucous membranes Line respiratory, digestive, and reproductive tracts; trap pathogens in sticky mucus Cilia Microscopic hair-like structures in the respiratory tract; move mucus (with trapped pathogens) upwards and out of the airways Stomach acid Hydrochloric acid (HCl) in the stomach (pH ~2) denatures proteins in pathogens and destroys most ingested bacteria Tears and saliva Contain lysozyme , an enzyme that breaks down peptidoglycan in bacterial cell walls, causing lysis Ear wax (cerumen) Traps pathogens and insects; contains antimicrobial properties Vaginal secretions Slightly acidic (pH ~4) due to lactic acid production by Lactobacillus ; inhibits growth of many pathogens Normal flora (microbiome) Commensal bacteria on the skin and in the gut compete with pathogens for nutrients and space; some produce antimicrobial substances
If pathogens breach the first line of defence, the second line provides a rapid, non-specific response.
1. Phagocytosis:
Phagocytes (neutrophils and macrophages) are white blood cells that engulf and destroy pathogens.
Phagocyte Type Source Location Characteristics Neutrophils Bone marrow; short-lived (hours) Blood; recruited to infection sites Most abundant phagocyte; first to arrive at infection; multi-lobed nucleus; granules contain digestive enzymes Macrophages Derived from monocytes Tissues (liver, lungs, lymph nodes, spleen) Larger and longer-lived than neutrophils; can present antigens to T cells (antigen-presenting cells); important in adaptive immunity
Stages of phagocytosis:
Chemotaxis: Phagocytes are attracted to the site of infection by chemical signals released by pathogens and damaged cells (e.g., cytokines, bacterial products)Recognition: Phagocyte receptors bind to molecules on the pathogen surface. Non-self molecules that trigger an immune response are called antigens . Phagocytes can also bind to pathogens that have been opsonised (coated with antibodies or complement proteins)Engulfment: The phagocyte extends pseudopodia around the pathogen, enclosing it in a membrane-bound vesicle called a phagosome Digestion: The phagosome fuses with a lysosome (containing digestive enzymes: lysozyme, proteases, lipases) to form a phagolysosome . Enzymes break down the pathogenExocytosis: Indigestible material is expelled from the cell by exocytosis2. Inflammation:
Inflammation is a localised response to tissue damage or infection. Its purpose is to isolate and destroy pathogens, remove damaged tissue, and initiate tissue repair.
The four cardinal signs of inflammation:
Sign Mechanism Redness Vasodilation increases blood flow to the area Heat Increased blood flow brings warm blood from the body core to the surface Swelling Increased permeability of capillary walls allows plasma proteins and fluid to leak into the tissue (oedema) Pain Swelling compresses nerve endings; inflammatory chemicals (prostaglandins, bradykinin) stimulate pain receptors
Sequence of events:
Tissue damage releases chemical mediators (histamine from mast cells, prostaglandins, cytokines) Histamine causes vasodilation and increased capillary permeability More blood flows to the area, bringing phagocytes (neutrophils first, then macrophages) Fluid and proteins leak into the tissue, causing swelling and helping to dilute toxins Phagocytes engulf and destroy pathogens Fibrin forms a clot around the area, walling off the infection 3. Fever (pyrexia):
Macrophages release cytokines called pyrogens that travel to the hypothalamus Pyrogens raise the hypothalamic set point, causing body temperature to increase Higher temperature inhibits pathogen growth (many pathogens grow best at 37 degrees C) Higher temperature increases metabolic rate, speeding up immune responses and tissue repair Extremely high fever (above 41 degrees C) is dangerous because it denatures human enzymes 4. Interferons:
Proteins produced by virus-infected cells They diffuse to neighbouring cells and stimulate them to produce antiviral proteins These antiviral proteins inhibit viral replication by degrading viral mRNA and blocking translation Interferons are NOT virus-specific — they provide broad-spectrum antiviral defence Adaptive immunity is a specific response to a particular pathogen. It is slower than innate immunity (takes several days to develop) but provides long-lasting protection through immunological memory .
Two types of adaptive immunity:
Type Cells Involved Target Mechanism Cell-mediated immunity T lymphocytes (T cells) Body’s own cells that are infected, cancerous, or transplanted Cytotoxic T cells directly destroy abnormal cells; T helper cells coordinate the immune response Humoral immunity B lymphocytes (B cells) Extracellular pathogens (bacteria, viruses outside cells, toxins) B cells differentiate into plasma cells that secrete antibodies specific to the pathogen’s antigens
An antigen is any molecule that can trigger an immune response. Most antigens are proteins or glycoproteins on the surface of pathogens.
Self-antigens: Molecules on the surface of the body’s own cells that are recognised as “self.” These do NOT normally trigger an immune response.Non-self antigens: Molecules on the surface of pathogens or foreign cells that are recognised as “non-self.” These DO trigger an immune response.Allergens: Harmless antigens (e.g., pollen, dust mite faeces, peanut proteins) that trigger an exaggerated immune response in sensitised individuals.T cells originate in the bone marrow but mature in the thymus gland .
T Cell Type Function Surface Marker T helper cells (C D 4 + \mathrm{CD4}^+ CD4 + Release cytokines that stimulate B cells to differentiate into plasma cells and memory cells; activate cytotoxic T cells and macrophages CD4 Cytotoxic T cells (C D 8 + \mathrm{CD8}^+ CD8 + Directly destroy virus-infected cells and cancer cells by inducing apoptosis (programmed cell death); recognise antigens presented on MHC class I CD8 Memory T cells Long-lived; provide rapid secondary response upon re-exposure to the same antigen — Regulatory T cells (Tregs) Suppress immune responses; prevent autoimmune reactions; maintain tolerance to self-antigens CD4, CD25
T cell activation:
Antigen presentation: Antigen-presenting cells (macrophages, dendritic cells, B cells) engulf pathogens, process their antigens, and display the antigens on their cell surface using MHC class II moleculesRecognition: A T helper cell with the specific receptor for that antigen binds to the antigen-MHC complexCo-stimulation: A second signal (from co-stimulatory molecules on the APC) is required to fully activate the T helper cellClonal expansion: The activated T helper cell divides by mitosis, producing many identical copies (clones) with the same antigen-specific receptorEffector function: The cloned T helper cells release cytokines that activate B cells and cytotoxic T cellsCytotoxic T cell action against virus-infected cells:
Virus-infected cells display viral antigens on their surface using MHC class I molecules A cytotoxic T cell with the matching receptor binds to the antigen-MHC I complex The cytotoxic T cell releases perforin , which forms pores in the target cell membrane Granzymes (enzymes) enter through the pores and activate caspases , which trigger apoptosis (programmed cell death)The virus inside the cell is destroyed along with the cell B cells originate and mature in the bone marrow .
B cell activation and antibody production:
Antigen recognition: A B cell with the specific surface receptor (membrane-bound antibody) binds to a free antigenAntigen internalisation: The B cell internalises the antigen and displays it on its surface using MHC class IIT helper cell interaction: An activated T helper cell with the matching receptor binds to the B cell’s antigen-MHC complex and releases cytokinesClonal expansion: The B cell divides by mitosis, producing many identical clonesDifferentiation: Most clones differentiate into plasma cells (short-lived, secrete large quantities of antibodies); some differentiate into memory B cells (long-lived, provide immunological memory)Structure of an antibody:
An antibody is a Y-shaped protein (immunoglobulin) composed of:
Two identical heavy chains (longer polypeptide chains)Two identical light chains (shorter polypeptide chains)Variable regions (at the tips of the Y): unique to each antibody type; determine which antigen the antibody can bind to (complementary shape)Constant regions (stem and base of the Y): the same for all antibodies of the same class; determine the antibody’s effector functionHinge region: allows flexibility, enabling the antibody to bind to antigens at different distancesHow antibodies work:
Mechanism Description Neutralisation Antibodies bind to the surface antigens of pathogens or toxins, blocking their ability to bind to host cells or enter tissues Agglutination Antibodies bind to multiple pathogens, clumping them together. This prevents them from spreading and makes it easier for phagocytes to engulf multiple pathogens at once Opsonisation Antibodies coat the surface of pathogens, marking them for phagocytosis. Phagocytes have receptors for the constant region of antibodies Complement activation Antibodies bound to pathogens trigger the complement system — a cascade of proteins that: (a) form membrane attack complexes (MAC) that lyse pathogens, (b) enhance inflammation, (c) promote opsonisation Precipitation Antibodies bind to soluble antigens (toxins), forming insoluble complexes that precipitate out of solution and are cleared by phagocytes
Feature Primary Response Secondary Response Trigger First exposure to an antigen Subsequent exposure to the SAME antigen Speed Slow: 5-10 days before antibody production peaks Fast: 1-3 days before antibody production peaks Antibody level Lower peak Much higher peak (10-100 times primary) Antibody class Mainly IgM initially, then IgG Mainly IgG (rapid, large-scale production) Duration Short-lived (weeks) Long-lived (months to years) Cells involved Naive B cells and T cells Memory B cells and memory T cells Result Symptoms of disease may develop before immunity is established no symptoms; pathogen destroyed rapidly
Immunological memory: After the primary response, memory B cells and memory T cells persist in the body for years or even a lifetime. Upon re-exposure to the same antigen, memory cells rapidly divide and differentiate into effector cells, producing a faster, stronger, and longer-lasting secondary response.
Vaccination exploits the immune system’s ability to develop immunological memory. By exposing the body to a harmless form of a pathogen (or its antigens), vaccination stimulates a primary immune response, producing memory cells without causing the disease.
Types of vaccine:
Vaccine Type Description Examples Live attenuated Weakened (attenuated) form of the pathogen; can replicate but does not cause disease in healthy individuals MMR (measles, mumps, rubella); BCG (tuberculosis) Inactivated (killed) Dead pathogen; cannot replicate; generally requires booster doses Influenza; polio (Salk vaccine); rabies Toxoid Inactivated toxin; stimulates antibody production against the toxin Tetanus; diphtheria Subunit (recombinant) Specific antigenic proteins from the pathogen HPV vaccine; Hepatitis B; COVID-19 (subunit) mRNA Messenger RNA that instructs cells to produce the pathogen’s antigen COVID-19 (Pfizer-BioNTech, Moderna) Viral vector Harmless virus engineered to carry genes for the pathogen’s antigen COVID-19 (Oxford-AstraZeneca, Janssen)
If a large proportion of a population is immune to a disease (through vaccination or previous infection), the spread of the pathogen is significantly reduced because there are fewer susceptible hosts. This provides indirect protection to individuals who are not immune (e.g., newborns, immunocompromised individuals).
Herd immunity threshold:
Threshold = ( 1 − 1 R 0 ) × 100 % \text{Threshold} = \left(1 - \frac{1}{R_0}\right) \times 100\% Threshold = ( 1 − R 0 1 ) × 100%
Where R 0 R_0 R 0
Disease R 0 R_0 R 0 Herd Immunity Threshold Measles 12-18 92-94% Polio 5-7 80-86% COVID-19 (Omicron) 8-12 87-92% Seasonal flu 1.5-3 33-67%
Advantages Risks and Limitations Provides individual immunity Rare adverse reactions (allergic reactions, fever) Protects vulnerable individuals (herd immunity) Some vaccines require multiple doses (boosters) Eliminates or eradicates diseases Not 100% effective in all individuals Cost-effective compared to treating disease Vaccine hesitancy and misinformation can reduce uptake Reduces antibiotic resistance Antigenic variation (mutations) in pathogens may require updated vaccines (e.g., annual flu vaccine)
In autoimmune diseases, the immune system mistakenly attacks the body’s own tissues (self-antigens), failing to distinguish between self and non-self.
Disease Target Tissue/Cells Symptoms Type 1 diabetes β \beta β Destruction of β \beta β Rheumatoid arthritis Synovial membranes of joints Joint inflammation, pain, swelling, cartilage destruction, deformity Multiple sclerosis (MS) Myelin sheath of neurons in the CNS Demyelination; impaired nerve conduction; muscle weakness, vision problems Lupus (SLE) Connective tissue, skin, kidneys, joints Butterfly rash, joint pain, kidney damage, fatigue Myasthenia gravis Acetylcholine receptors at neuromuscular junctions Muscle weakness that worsens with activity; drooping eyelids, difficulty swallowing Coeliac disease Villi of the small intestine (triggered by gluten) Damage to intestinal villi; malabsorption; diarrhoea, weight loss
Possible causes of autoimmune disease:
Genetic predisposition (certain HLA genes are associated with autoimmune conditions) Environmental triggers (infections, stress, hormones) Molecular mimicry: some pathogens have antigens similar to self-antigens; antibodies produced against the pathogen cross-react with the body’s own tissues An allergy is an exaggerated immune response to a harmless antigen (allergen). The most common type is Type I hypersensitivity (IgE-mediated).
Mechanism of an allergic response:
Sensitisation (first exposure): The allergen enters the body for the first time. B cells produce IgE antibodies against the allergen. IgE binds to the surface of mast cells (in connective tissue) and basophils (in blood).Re-exposure: Upon subsequent exposure, the allergen binds to the IgE antibodies on mast cells, cross-linking them.Degranulation: The mast cells release histamine and other inflammatory mediators (degranulation).Symptoms: Histamine causes vasodilation, increased capillary permeability (swelling), mucus production, and smooth muscle contraction (bronchoconstriction).Allergic Condition Symptoms Hay fever (allergic rhinitis) Sneezing, runny nose, itchy eyes, nasal congestion (pollen allergen) Asthma Wheezing, difficulty breathing, bronchoconstriction (dust mites, pollen, pet dander) Anaphylaxis Life-threatening: airway constriction, drop in blood pressure, swelling of tongue/throat Eczema (atopic dermatitis) Red, itchy, inflamed skin Food allergy Hives, swelling, gastrointestinal symptoms, anaphylaxis (peanuts, shellfish, eggs)
Treatment of allergies:
Antihistamines: Block histamine receptors, reducing symptomsAdrenaline (epinephrine): Used for anaphylaxis — constricts blood vessels, opens airways, increases heart rateCorticosteroids: Reduce inflammationDesensitisation (immunotherapy): Gradual exposure to increasing doses of the allergen to induce tolerance (shifts immune response from IgE to IgG)Human Immunodeficiency Virus (HIV):
Feature Description Pathogen type Retrovirus (RNA virus) that carries reverse transcriptase Target cells T helper cells (C D 4 + \mathrm{CD4}^+ CD4 + Transmission Unprotected sexual contact; contaminated blood products; sharing needles; mother-to-child (during birth or breastfeeding) Not transmitted by Casual contact, hugging, sharing utensils, mosquito bites
HIV lifecycle:
HIV binds to CD4 receptors and co-receptors (CCR5 or CXCR4) on T helper cells The viral envelope fuses with the host cell membrane Viral RNA and reverse transcriptase enter the cell Reverse transcriptase converts viral RNA into viral DNA Viral DNA is integrated into the host cell’s genome by integrase The host cell uses its own machinery to transcribe and translate the viral genes, producing new viral proteins New viral particles are assembled and bud from the cell membrane, acquiring an envelope The new viruses infect other T helper cells Stages of HIV infection:
Stage Description Acute infection 2-4 weeks after exposure; flu-like symptoms; high viral load; T helper cell count drops briefly then partially recovers Clinical latency May last 8-10 years; no symptoms; virus replicates slowly; T helper cell count gradually declines AIDS T helper cell count drops below 200 cells/mm3 ^3 3
Opportunistic infections in AIDS:
Pneumocystis jirovecii pneumonia (fungal lung infection)Mycobacterium tuberculosis (tuberculosis)Kaposi’s sarcoma (cancer caused by human herpesvirus 8) Candidiasis (thrush) Cytomegalovirus (CMV) infections Treatment and prevention:
Antiretroviral therapy (ART): Combination of drugs targeting different stages of the HIV lifecycle: reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors, fusion inhibitors. ART does not cure HIV but can reduce viral load to undetectable levels, preventing AIDS and transmission.Prevention: Safe sex (condoms); needle exchange programmes; pre-exposure prophylaxis (PrEP); screening of blood products; avoiding sharing needles; mother-to-child transmission prevention (ART during pregnancy and delivery)Monoclonal antibodies are identical antibodies produced by a single clone of B cells (plasma cells). They are all specific to the same antigen.
Production (using hybridoma technology):
A mouse is injected with the target antigen, stimulating B cells to produce antibodies B cells are extracted from the mouse’s spleen B cells are fused with myeloma cells (cancerous B cells that divide indefinitely) using polyethylene glycol The resulting hybridoma cells have the antibody-producing ability of B cells and the immortality of cancer cells Hybridoma cells are cultured; each clone produces one specific antibody The desired clone is selected and grown in large-scale culture Antibodies are extracted and purified Applications:
Application Description Medical diagnosis Pregnancy tests (detect hCG); detection of specific pathogens or disease markers in blood samples Cancer treatment Monoclonal antibodies designed to bind to specific cancer cell antigens, marking them for destruction by the immune system Autoimmune disease Infliximab (binds to and neutralises TNF-alpha, reducing inflammation in rheumatoid arthritis and Crohn’s disease) COVID-19 treatment Monoclonal antibody cocktails that bind to the SARS-CoV-2 spike protein, neutralising the virus
ELISA is a widely used biochemical technique that uses antibodies and colour change to detect and quantify specific antigens (or antibodies) in a sample.
Direct ELISA (detecting antigen):
The specific antibody is attached to the bottom of a well in a microtitre plate The patient’s sample (potentially containing the target antigen) is added to the well If the antigen is present, it binds to the antibody on the plate The well is washed to remove unbound material A second antibody, linked to an enzyme, is added. This antibody binds to a different epitope on the antigen (forming a “sandwich”) The well is washed again A substrate is added that the enzyme converts to a coloured product The intensity of the colour is measured with a spectrophotometer and is proportional to the amount of antigen in the sample Indirect ELISA (detecting antibodies — used in HIV testing):
The specific antigen is attached to the bottom of a well The patient’s blood serum (potentially containing antibodies against the antigen) is added If the target antibody is present, it binds to the antigen The well is washed to remove unbound antibodies A secondary antibody (anti-human immunoglobulin) linked to an enzyme is added; it binds to the patient’s antibody The well is washed again Substrate is added; enzyme converts it to a coloured product Colour intensity indicates the amount of antibody in the sample Application Target Description Disease diagnosis HIV antibodies; hepatitis B surface antigen; SARS-CoV-2 antibodies Detects exposure to specific pathogens Pregnancy testing hCG (human chorionic gonadotropin) Detects the hormone produced during early pregnancy in urine or blood Allergy testing IgE antibodies specific to allergens Measures the level of allergen-specific IgE in blood Drug testing Specific drug molecules Detects drugs or their metabolites in blood or urine Food safety Food allergens, pathogens Detects traces of allergens (peanut protein) or bacteria (Salmonella , E. Coli ) in food samples Environmental monitoring Toxins, pollutants Measures levels of environmental contaminants in water or soil samples
Category Type Description Example Active Natural The body produces its own antibodies after natural exposure to a pathogen Recovering from chickenpox provides immunity to future infection Active Artificial The body produces its own antibodies after vaccination MMR vaccine provides immunity to measles, mumps, and rubella Passive Natural Pre-formed antibodies are transferred from mother to baby across the placenta (IgG) or in breast milk (IgA/sIgA) Newborn immunity to diseases the mother has had Passive Artificial Pre-formed antibodies are injected into the body (from an immune animal or human donor) Antivenom for snake bite; rabies immunoglobulin; tetanus antitoxin
Feature Active Immunity Passive Immunity Antibody source Body’s own plasma cells Pre-formed antibodies from another source Memory cells Produced (long-lasting protection) NOT produced (short-lived protection) Onset Slow (days to weeks) Immediate (instant protection) Duration Long-lasting (years to lifetime) Short-lived (weeks to months) Boosters Booster doses extend immunity Cannot be boosted (no memory cells)
and between natural and artificial immunity. Remember: “active” means the body MAKES its own antibodies; “passive” means the body RECEIVES pre-made antibodies. “Natural” means the exposure occurred (infection or maternal transfer); “artificial” means the exposure was deliberate (vaccination or antibody injection).
Confusing antigens and antibodies: Antigens are molecules on the surface of pathogens (or other foreign substances) that trigger an immune response. Antibodies are proteins produced by plasma cells that bind to specific antigens. Antigens are the “target”; antibodies are the “weapon.”
Writing that phagocytes are specific: Phagocytosis is a NON-SPECIFIC (innate) response. Phagocytes engulf any foreign material, not just a specific pathogen. Specificity is the feature of adaptive immunity (B cells and T cells).
Confusing T cells and B cells: T cells mature in the THYMUS; B cells mature in the BONE MARROW. T cells are involved in cell-mediated immunity (directly killing infected cells); B cells are involved in humoral immunity (producing antibodies). T helper cells HELP B cells; they do not produce antibodies themselves.
Writing that antibodies directly kill pathogens: Antibodies do NOT kill pathogens directly. They work by neutralising, agglutinating, opsonising (marking for phagocytosis), activating complement, or precipitating. The actual killing is done by phagocytes, complement proteins, or cytotoxic T cells.
Confusing memory cells with plasma cells: Plasma cells are short-lived (days to weeks) and secrete large quantities of antibodies during the primary response. Memory cells are long-lived (years) and do NOT secrete antibodies until re-exposure triggers a secondary response.
Writing that antibiotics treat viral infections: Antibiotics target bacterial structures (cell wall, ribosomes) that viruses do not have. Antibiotics are ineffective against viruses. Antiviral drugs (e.g., reverse transcriptase inhibitors for HIV) are used to treat viral infections.
Confusing IgM and IgG: IgM is the FIRST antibody produced in the primary response; it is a large pentamer (5 antibody units) that is effective at agglutination. IgG is the MAIN antibody in the secondary response; it is smaller (monomer), crosses the placenta, and provides long-term immunity.
Writing that HIV directly kills the host: HIV does not directly cause death. It destroys T helper cells, which are essential for coordinating the immune response. Without T helper cells, the immune system collapses, and the person becomes susceptible to opportunistic infections that ultimately cause death.
Confusing the roles of perforin and antibodies: Perforin is released by CYTOTOXIC T CELLS and forms pores in the membrane of infected cells. Antibodies are produced by PLASMA CELLS and bind to free pathogens. They are different components of the immune response.
Writing that vaccination provides passive immunity: Vaccination provides ACTIVE artificial immunity (the person’s own immune system produces antibodies and memory cells). Passive immunity involves receiving pre-formed antibodies from another source (e.g., maternal antibodies crossing the placenta, antivenom injections).
Problem 1: Describe the stages of phagocytosis. Explain how the innate immune system and the adaptive immune system work together to eliminate a bacterial infection.
If you get this wrong, revise: Innate Immunity — Phagocytosis; Adaptive Immunity — T Cells and B Cells
Solution Stages of phagocytosis:
Chemotaxis: Phagocytes are attracted to chemical signals (cytokines, bacterial products) released at the infection site.Recognition: Phagocyte receptors bind to antigens on the bacterial surface (or to antibodies/complement coating the bacteria — opsonisation).Engulfment: Pseudopodia extend around the bacterium, enclosing it in a phagosome.Digestion: The phagosome fuses with a lysosome to form a phagolysosome. Enzymes (lysozyme, proteases) break down the bacterium.Exocytosis: Indigestible material is expelled from the cell.Cooperation between innate and adaptive immunity:
Macrophages (innate) phagocytose bacteria and become antigen-presenting cells. They display bacterial antigens on their surface using MHC class II molecules. A T helper cell (adaptive) with the matching receptor recognises the antigen-MHC complex and is activated. The activated T helper cell releases cytokines that stimulate B cells to produce antibodies specific to the bacteria. These antibodies (adaptive) then opsonise more bacteria, making them easier for phagocytes (innate) to engulf. This cooperation enhances the overall effectiveness of the immune response.
Problem 2: Explain the difference between the primary and secondary immune responses. Why does the secondary response provide better protection against disease?
If you get this wrong, revise: Adaptive Immunity — Primary and Secondary Immune Responses
Solution The primary response occurs on first exposure to an antigen. It is slow (5-10 days to peak antibody production), produces a lower peak of antibodies (mainly IgM initially), and the person may experience symptoms of disease before immunity is established. Clonal expansion of naive B and T cells takes time.
The secondary response occurs on subsequent exposure to the SAME antigen. It is fast (1-3 days to peak), produces a much higher peak of antibodies (mainly IgG, 10-100 times more than primary), and provides rapid protection before symptoms develop. This is because memory B cells and memory T cells produced during the primary response persist in the body. Upon re-exposure, memory cells rapidly divide and differentiate into effector cells (plasma cells and cytotoxic T cells) without needing to go through the slow initial activation process. The pathogen is destroyed before it can multiply enough to cause disease.
Problem 3: A person is bitten by a snake and requires antivenom. Explain why the antivenom provides only temporary protection and does not provide long-term immunity. Contrast this with the protection provided by a tetanus vaccine.
If you get this wrong, revise: Antibodies — Types of Immunity; Vaccination
Solution Antivenom contains pre-formed antibodies against the snake venom. This is passive artificial immunity — the person receives antibodies produced by another organism ( a horse or sheep that has been injected with snake venom). These antibodies circulate in the blood, neutralising the venom. However, the antibodies are NOT produced by the person’s own immune system, so no memory B cells are generated. The antibodies are gradually broken down by the body (within weeks), and the person is not protected against future snake bites. If bitten again, they would need another dose of antivenom.
In contrast, a tetanus vaccine contains a toxoid (inactivated tetanus toxin). This stimulates the person’s own immune system to produce a primary response, generating memory B cells and memory T cells. If the person is later exposed to tetanus toxin (from a wound contaminated with Clostridium tetani ), memory cells mount a rapid secondary response, producing large quantities of antibodies that neutralise the toxin before it causes symptoms. This is active artificial immunity and provides long-lasting protection (booster doses every 10 years).
Human Immunodeficiency Virus (HIV) is a retrovirus — an RNA virus that carries reverse transcriptase, enabling it to convert its RNA genome into DNA, which integrates into the host cell’s chromosomes.
Feature Description Pathogen type Retrovirus (RNA virus with reverse transcriptase) Target cells T helper cells (C D 4 + \mathrm{CD4}^+ CD4 + Genetic material Two copies of single-stranded RNA; nine genes (gag, pol, env, tat, rev, nef, vif, vpr, vpu) Viral envelope Stolen from host cell membrane during budding; contains viral glycoproteins gp120 (binds CD4 receptor) and gp41 (mediates fusion) Transmission Unprotected sexual contact; contaminated blood products; sharing needles; mother-to-child (during birth or breastfeeding) Not transmitted by Casual contact, hugging, sharing utensils, mosquito bites, swimming pools
HIV lifecycle:
Attachment: gp120 on the viral envelope binds to CD4 receptors and a co-receptor (CCR5 or CXCR4) on the target cell surfaceFusion: gp41 mediates fusion of the viral envelope with the host cell membrane, and the viral capsid enters the cellReverse transcription: Reverse transcriptase converts the viral RNA genome into double-stranded viral DNAIntegration: Viral integrase inserts the viral DNA into the host cell’s chromosomes at a random location (provirus)Latency: The proviral DNA may remain dormant (latent) for years, producing no new viral particles. During latency, the person is HIV-positive but may show no symptomsActivation: When the T cell is activated, transcription of the proviral DNA begins, producing viral mRNA and genomic RNATranslation: Host ribosomes translate viral mRNA into viral proteins (gag, pol, env)Assembly: New viral particles assemble at the cell membraneBudding: New viruses bud from the host cell membrane, acquiring an envelope, and go on to infect other cellsStage Description CD4 count (/mm3 ^3 3 Acute infection Flu-like symptoms 2-4 weeks after exposure; high viral load; CD4 count drops briefly then partially recovers 500-1000 (may drop below 200) Clinical latency May last 8-10 years; no symptoms; virus replicates slowly; CD4 gradually declines 200-500 AIDS CD4 falls below 200; immune system severely compromised; opportunistic infections develop Below 200
Opportunistic infections in AIDS:
Infection Pathogen Type Description Pneumocystis jirovecii pneumoniaFungus Fatal without treatment; causes coughing, fever, shortness of breath Tuberculosis Mycobacterium tuberculosis Reactivation of latent TB is common in HIV/AIDS patients Kaposi’s sarcoma Human herpesvirus 8 (HHV-8) Cancer of blood vessel cells; causes purple skin lesions Candidiasis (thrush) Candida albicans Fungal infection of mouth, oesophagus, vagina Cytomegalovirus (CMV) Cytomegalovirus (HHV-5) Can cause retinitis (blindness), colitis, pneumonia
Antiretroviral therapy (ART):
Drug class Example Mechanism NRTIs AZT, lamivudine (3TC) Competitive inhibitors of reverse transcriptase; cause chain termination during DNA synthesis NNRTIs Efavirenz, nevirapine Bind to and inhibit reverse transcriptase at an allosteric site PIs Ritonavir, indinavir Inhibit HIV protease; prevent processing of viral polyproteins into functional proteins Integrase inhibitors Raltegravir Block integrase; prevent integration of viral DNA into host chromosomes Entry inhibitors Maraviroc Block CCR5 co-receptor; prevent HIV from entering T cells
ART does not cure HIV but can reduce viral load to undetectable levels, preventing AIDS and allowing near-normal life expectancy. Combination therapy (3 or more drugs from at least 2 classes) is standard practice to prevent resistance.
Prevention: Condoms; needle exchange programmes; pre-exposure prophylaxis (PrEP); screening blood products; avoiding sharing needles; mother-to-child transmission prevention with ART during pregnancy and delivery.
In autoimmune diseases, the immune system fails to distinguish between self-antigens and non-self antigens, attacking the body’s own tissues.
Possible causes:
Molecular mimicry: Pathogens have antigens similar to self-antigens; antibodies produced against the pathogen cross-react with self-tissuesGenetic predisposition: Certain HLA genes are associated with autoimmune conditionsEnvironmental triggers: Infections, stress, hormones may trigger onset in genetically susceptible individualsEpigenetic factors: Environmental exposures may alter gene expression in immune cellsDisease Target Tissue/Cells Symptoms Type 1 diabetes β \beta β Destruction of β \beta β Rheumatoid arthritis Synovial membranes of joints Joint inflammation, pain, swelling, cartilage destruction, deformity Multiple sclerosis (MS) Myelin sheath of neurons in the CNS Demyelination; impaired nerve conduction; muscle weakness, vision problems Systemic lupus erythematosus (SLE) Connective tissue, skin, kidneys, joints Butterfly rash, joint pain, kidney damage, fatigue Myasthenia gravis Acetylcholine receptors at neuromuscular junctions Muscle weakness that worsens with activity; drooping eyelids, difficulty swallowing Coeliac disease Villi of the small intestine (triggered by gluten) Damage to intestinal villi; malabsorption; diarrhoea, weight loss Hashimoto’s thyroiditis Thyroid gland Hypothyroidism; weight gain, fatigue, cold intolerance, goitre
Approach Description Immunosuppressants Drugs that suppress immune system activity (e.g., corticosteroids, methotrexate, cyclosporine) Anti-inflammatory drugs NSAIDs (e.g., ibuprofen) for pain and inflammation Replacement therapy Insulin for Type 1 diabetes; thyroxine for Hashimoto’s thyroiditis Monoclonal antibodies Targeted antibodies that block specific immune pathways (e.g., anti-TNF-alpha for rheumatoid arthritis) Plasmapheresis Filtering blood to remove autoantibodies and immune complexes
which covers immune system topics within the DSE specification.
See for instructions on self-marking and building a personal test matrix.
Type I hypersensitivity (immediate hypersensitivity) is the mechanism underlying allergic reactions:
Sensitisation: On first exposure to an allergen (e.g., pollen, dust mite faeces, peanut protein), the allergen is taken up by antigen-presenting cells (APCs) and presented to T helper cellsTh2 response: T helper cells differentiate into Th2 cells, which release cytokines (IL-4, IL-5, IL-13) that stimulate B cells to produce IgE antibodies specific to the allergenIgE binding: The IgE antibodies bind to Fc receptors on the surface of mast cells (in connective tissue) and basophils (in blood). The person is now “sensitised” — no symptoms occur on this first exposureRe-exposure: On subsequent exposure to the same allergen, the allergen cross-links the IgE antibodies on mast cells/basophilsDegranulation: Cross-linking triggers mast cells to degranulate — releasing pre-formed mediators stored in granules:Histamine: Causes vasodilation, increased capillary permeability (leading to swelling, redness, heat), mucus secretion, smooth muscle contraction (bronchoconstriction in the airways), itchingHeparin: Prevents blood clotting at the site of inflammationSerotonin (5-HT): Contributes to inflammation and smooth muscle contractionLate-phase response: Hours later, newly synthesised mediators are released (leukotrienes, prostaglandins, cytokines), causing sustained inflammationSymptom Cause Treatment Hay fever (allergic rhinitis) Histamine causes vasodilation and mucus secretion in nasal passages Antihistamines; corticosteroid nasal sprays Asthma Histamine and leukotrienes cause bronchoconstriction and mucus secretion in airways Bronchodilators (salbutamol); inhaled corticosteroids; leukotriene receptor antagonists Eczema (atopic dermatitis) Inflammatory response in the skin; dry, itchy, red patches Moisturisers; topical corticosteroids; antihistamines Anaphylaxis Systemic release of histamine; massive vasodilation causing drop in blood pressure; airway constriction; swelling of throat Adrenaline (epinephrine) auto-injector (EpiPen); call emergency services
Competitive antagonists of histamine at H1 receptors They bind to H1 receptors on target cells (blood vessels, smooth muscle, nerve endings) without activating them This prevents histamine from binding and exerting its effects First-generation antihistamines (e.g., diphenhydramine): cross the blood-brain barrier, cause drowsinessSecond-generation antihistamines (e.g., cetirizine, loratadine): do not readily cross the blood-brain barrier, minimal sedationBlood Group Antigens on RBC Surface Antibodies in Plasma Can Donate To Can Receive From A A Anti-B A, AB A, O B B Anti-A B, AB B, O AB A and B Neither AB A, B, AB, O (universal recipient) O Neither Anti-A and Anti-B A, B, AB, O (universal donor) O
Agglutination: If incompatible blood is transfused, antibodies in the recipient’s plasma bind to antigens on the donor’s red blood cells, causing them to clump (agglutinate). This blocks blood vessels and triggers complement-mediated lysis of the RBCs, which can be fatal.
The RhD antigen is another antigen on the surface of red blood cells Individuals who have the RhD antigen are Rh-positive (Rh+) ; those who do not are Rh-negative (Rh-) Rh-negative individuals can produce anti-Rh antibodies if exposed to Rh-positive blood (e.g., during pregnancy or transfusion) Haemolytic disease of the newborn (HDN):
An Rh-negative mother carries an Rh-positive foetus (inherited from the father) During the first pregnancy, foetal Rh-positive red blood cells may cross into the maternal circulation ( during delivery) The mother’s immune system produces anti-Rh antibodies In a subsequent pregnancy with another Rh-positive foetus, maternal anti-Rh antibodies (IgG) can cross the placenta These antibodies bind to foetal Rh-positive RBCs, causing agglutination and complement-mediated lysis (haemolysis) This leads to haemolytic disease of the newborn (erythroblastosis fetalis): anaemia, jaundice, brain damage, or death of the foetus Prevention: Administration of anti-RhD immunoglobulin (RhoGAM) to the Rh-negative mother within 72 hours of delivery. This antibody binds to and destroys any foetal Rh-positive RBCs in the maternal circulation before the mother’s immune system can produce its own antibodiesFor a tissue or organ transplant to be successful, the donor and recipient must be as genetically similar as possible to minimise immune rejection.
Type of Match Description Rejection Risk Autograft Tissue transplanted from one part of a person’s body to another None Isograft Tissue transplanted between genetically identical individuals (identical twins) None Allograft Tissue transplanted between genetically non-identical individuals of the same species High Xenograft Tissue transplanted from a different species Very high
Types of rejection:
Type Timing Mechanism Hyperacute rejection Minutes to hours Pre-existing antibodies in the recipient immediately attack the donor tissue; caused by ABO or HLA incompatibility Acute rejection Days to weeks T cells recognise foreign HLA antigens on donor cells and mount a cell-mediated immune response Chronic rejection Months to years Gradual T cell and antibody-mediated damage; fibrosis and scarring of the transplanted tissue
Immunosuppressive drugs (e.g., ciclosporin, tacrolimus, corticosteroids) are given to transplant recipients to suppress the immune response and prevent rejection. However, these drugs also increase susceptibility to infections.
The lymphatic system is a network of vessels, tissues, and organs that:
Returns excess interstitial fluid to the blood (prevents tissue swelling/oedema) Transports dietary lipids from the small intestine to the blood (via lacteals in villi) Provides a pathway for immune cells (lymphocytes, macrophages) to travel throughout the body Filters lymph at lymph nodes, trapping pathogens, dead cells, and cellular debris Feature Description Structure Thin-walled vessels with valves (similar to veins); carry lymph (a clear fluid similar to blood plasma but without RBCs and platelets) Flow direction One-way: from tissues towards the heart; lymph drains into the subclavian veins via the thoracic duct (left) and right lymphatic duct Pumping mechanism Lymph is moved by contraction of surrounding skeletal muscles, breathing movements, and valves that prevent backflow Capillaries Lymphatic capillaries are blind-ended and more permeable than blood capillaries; they allow larger molecules (proteins, cell debris) to enter
Small, bean-shaped structures distributed along lymphatic vessels Filter lymph as it passes through Contain lymphocytes (B cells and T cells) and macrophages During an infection, lymph nodes become swollen and tender (e.g., swollen glands in the neck during a throat infection) Major lymph node groups: cervical (neck), axillary (armpits), inguinal (groin), mesenteric (abdomen) Organ Location Function Spleen Upper left abdomen Filters blood; removes old/damaged RBCs; stores platelets; contains lymphocytes; responds to blood-borne pathogens Thymus Upper chest (behind sternum) Site of T cell maturation; T cells migrate from bone marrow to thymus where they undergo selection (positive and negative); atrophies after puberty Tonsils Throat (pharynx) Trap pathogens entering through the mouth and nose; contain lymphocytes; often removed if chronically infected Peyer’s patches Small intestine Aggregates of lymphoid tissue in the intestinal wall; monitor intestinal bacteria and pathogens; part of GALT (gut-associated lymphoid tissue)
Vaccine Type Description Examples Advantages Disadvantages Live attenuated Weakened form of the pathogen; can replicate but cannot cause disease in healthy individuals MMR (measles, mumps, rubella); BCG (tuberculosis); oral polio Strong immune response; often lifelong immunity with 1-2 doses Cannot be given to immunocompromised individuals; risk of reversion to virulence Inactivated (killed) Pathogen is killed by heat or chemicals; cannot replicate Influenza (injectable); hepatitis A; cholera Safer than live vaccines; no risk of reversion Weaker immune response; requires booster doses; often requires adjuvant Toxoid Inactivated toxin produced by the pathogen; immune response targets the toxin, not the pathogen Tetanus; diphtheria Effective against toxin-mediated diseases Requires booster doses (every 10 years for tetanus) Subunit (recombinant) Purified antigenic components of the pathogen (specific proteins) Hepatitis B; HPV; acellular pertussis Very safe; well-defined composition Weaker immune response; more expensive to produce Conjugate Polysaccharide antigens linked to a carrier protein; improves immune response in young children Hib (Haemophilus influenzae type b); pneumococcal; meningococcal Effective in infants and young children More complex to manufacture mRNA Synthetic mRNA encoding a pathogen antigen; host cells translate the mRNA to produce the antigen, triggering an immune response COVID-19 (Pfizer, Moderna) Rapid development; strong immune response; no live pathogen used Requires cold storage; relatively new technology Viral vector Harmless virus engineered to carry genes encoding a pathogen antigen; the vector delivers the gene to host cells, which produce the antigen COVID-19 (AstraZeneca, Janssen); Ebola Strong immune response; no live pathogen Pre-existing immunity to the vector may reduce effectiveness
When a sufficiently high proportion of a population is immune to a disease (through vaccination or previous infection), the spread of the disease is significantly reduced, providing indirect protection to those who are not immune The herd immunity threshold depends on the basic reproduction number (R 0 R_0 R 0 Herd immunity threshold = 1 − 1 R 0 \text{Herd immunity threshold} = 1 - \frac{1}{R_0} Herd immunity threshold = 1 − R 0 1
Disease R 0 R_0 R 0 Herd Immunity Threshold Measles 12-18 92-94% Polio 5-7 80-86% COVID-19 (Omicron) 8-10 87-90% Influenza 1.5-3 33-67% Diphtheria 4-6 75-83%
IgE is involved in allergic reactions, NOT IgG or IgM. IgE binds to mast cells and basophils; cross-linking triggers degranulationHistamine causes vasodilation and increased permeability, NOT vasoconstriction. The result is swelling, redness, and heatRh-negative mothers are given anti-RhD immunoglobulin AFTER delivery, not before. This prevents sensitisation to Rh-positive foetal RBCs that entered maternal circulation during deliveryUniversal donor = O negative (not just O). The donor must be negative for both ABO and Rh antigensVaccines contain antigens, NOT antibodies. Vaccines stimulate the body to produce its own antibodies and memory cellsFeature Innate Immunity Adaptive (Acquired) Immunity Speed of response Immediate (minutes to hours) Slower (days to weeks); requires clonal selection and expansion Specificity Non-specific; responds to a broad range of pathogens in the same way Highly specific; produces antibodies and T cells targeted to specific antigens Memory No immunological memory; responds identically on each exposure Immunological memory; second exposure produces a faster, stronger response Components Physical barriers (skin, mucous membranes); phagocytes (neutrophils, macrophages); complement system; natural killer cells; inflammation B lymphocytes (antibodies); T lymphocytes (helper T cells, cytotoxic T cells, memory cells) Types of molecules involved Pattern recognition receptors (PRRs) that recognise pathogen-associated molecular patterns (PAMPs) — broad molecular patterns shared by many pathogens B cell receptors (BCRs) and T cell receptors (TCRs) that recognise specific antigen epitopes — unique molecular shapes Effectiveness Effective against a wide range of pathogens but can be overwhelmed; does not improve with repeated exposure Highly effective; improves with each exposure (affinity maturation, memory cells)
Feature Primary Response Secondary Response Trigger First exposure to a specific antigen Subsequent exposure to the SAME antigen Lag phase Longer (5-10 days); time needed for clonal selection, expansion, and differentiation of B and T cells Shorter (1-3 days); memory cells already exist and respond quickly Antibody concentration Lower peak; IgM produced first, then IgG Higher peak; mainly IgG (due to class switching); peak antibody level is much higher (10-100x primary response) Antibody affinity Lower affinity (antibodies bind less tightly to the antigen) Higher affinity (antibodies bind more tightly; affinity maturation has occurred during primary response via somatic hypermutation) Duration Shorter; antibody levels decline relatively quickly after the peak Longer; antibody levels remain elevated for weeks to months Memory cells Memory B and T cells are produced during the primary response Memory cells from the primary response are immediately activated; no need for clonal selection Clinical significance The person may experience symptoms of the disease while the immune system is mounting its response The person is protected from the disease; may have mild or no symptoms (immunity)
Feature Description Pathogen Plasmodium falciparum (most severe), P. Vivax , P. Ovale , P. Malariae (protozoan parasite)Vector Female Anopheles mosquito (transmits the parasite when it takes a blood meal) Lifecycle (1) Infected mosquito injects Plasmodium sporozoites into the human bloodstream → \rightarrow → → \rightarrow → → \rightarrow → → \rightarrow → → \rightarrow → → \rightarrow → → \rightarrow → Symptoms Recurring fever (every 48-72 hours, corresponding to RBC bursting cycles), chills, sweating, headache, nausea, anaemia, splenomegaly (enlarged spleen) Prevention Mosquito nets (insecticide-treated); antimalarial drugs (prophylaxis); mosquito control (draining breeding sites, insecticide spraying); vaccine (RTS,S — partially effective) Treatment Artemisinin-based combination therapies (ACTs); quinine (for severe cases) Global impact ~240 million cases per year; ~600,000 deaths per year (mostly children under 5 in sub-Saharan Africa)
Feature Description Pathogen Mycobacterium tuberculosis (bacterium)Transmission Airborne droplets (coughing, sneezing); close and prolonged contact with an infected person Primary infection Bacteria are inhaled and engulfed by macrophages in the alveoli; the bacteria can survive and multiply INSIDE the macrophages (they resist destruction by inhibiting phagosome-lysosome fusion) Latent TB In most healthy individuals, the immune system walls off the infection in a granuloma (a collection of immune cells surrounding the bacteria); the person has no symptoms and is not infectious; the bacteria can remain dormant for years Active TB If the immune system weakens, the bacteria reactivate and multiply; symptoms include persistent cough (sometimes blood-tinged sputum), weight loss, night sweats, fever, fatigue Treatment Combination antibiotic therapy (isoniazid, rifampicin, pyrazinamide, ethambutol) for at least 6 months; drug resistance is a growing problem (MDR-TB, XDR-TB) Prevention BCG vaccine (provides partial protection, especially against severe TB in children); improved living conditions; infection control DOTS programme Directly Observed Treatment, Short-course — WHO strategy to ensure patients complete their full course of treatment
Feature Description Pathogen Vibrio cholerae (bacterium; curved, rod-shaped, flagellated)Transmission Faecal-oral route; contaminated water and food (especially in areas with poor sanitation) Mechanism V. Cholerae attaches to the intestinal wall and produces cholera toxin; the toxin causes chloride ion channels in the intestinal epithelial cells to remain open; chloride ions are secreted into the intestinal lumen; sodium ions and water follow by osmosis; massive volumes of watery diarrhoea result (up to 20 litres per day)Symptoms Profuse, painless, watery diarrhoea (“rice-water stools”); vomiting; rapid dehydration; electrolyte imbalance; can be fatal within hours if untreated Treatment Oral rehydration therapy (ORT): a solution of clean water, glucose, sodium chloride, and potassium chloride is given orally; the glucose facilitates the co-transport of sodium ions back into the epithelial cells (using SGLT1 transporters), and water follows by osmosis; antibiotics (tetracycline) reduce the duration and severity Prevention Clean water supply; proper sanitation; hand hygiene; vaccination (oral cholera vaccine)
Feature Description Why HIV is hard to cure (1) High mutation rate: reverse transcriptase has no …/1-number-and-algebra/3_proof-and-logicreading function, so many mutations occur; this creates viral variants that can evade the immune system and develop drug resistance. (2) Latency: HIV integrates into the host genome as a provirus and can remain dormant for years, invisible to the immune system and unaffected by antiretroviral drugs that target active viral replication. (3) Reservoirs: HIV persists in reservoirs such as lymph nodes, the brain, and the gut-associated lymphoid tissue (GALT), where drugs may not reach effective concentrations. (4) Destruction of CD4+ T cells: HIV specifically targets and destroys the immune cells needed to fight it, progressively weakening the immune system ”Berlin Patient” Timothy Ray Brown, the first person cured of HIV (2011). He received a bone marrow transplant from a donor with a CCR5-delta32 mutation (a natural genetic mutation that makes cells resistant to HIV because the CCR5 co-receptor is non-functional). This demonstrated that a cure is theoretically possible, but bone marrow transplantation is too risky and expensive for widespread use ”London Patient” Adam Castillejo, the second person cured of HIV (2019). Similar approach: bone marrow transplant from a CCR5-delta32 donor for Hodgkin’s lymphoma treatment
Prepare a bacterial lawn on an agar plate (spread a known volume of bacterial culture evenly across the surface) Using sterile forceps, place antibiotic discs (or discs soaked in different concentrations of an antibiotic) onto the agar surface Incubate the plate at an appropriate temperature (e.g., 30 degrees C for environmental bacteria, 37 degrees C for human pathogens) for 24-48 hours Measure the zone of inhibition (the clear area around each disc where bacteria have been killed or their growth has been inhibited) A larger zone of inhibition indicates greater effectiveness of the antibiotic against that bacterium Compare zones of inhibition between different antibiotics to determine which is most effective Controls:
Positive control: an antibiotic disc with a known effective antibiotic (confirms the bacteria are susceptible to some antibiotics) Negative control: a disc with no antibiotic (confirms that the bacteria can grow on the agar and that the clear zone is caused by the antibiotic, not by the disc itself) ::: An army within: The immune system is like a defense force — white blood cells are soldiers, antibodies are targeted weapons, and memory cells are intelligence officers who remember past invaders.
Why it matters: From vaccines to autoimmune diseases, immunology explains how the body fights disease and sometimes mistakenly attacks itself.
The key insight: Immunity has two branches — innate (fast, general) and adaptive (slow, specific) — working together provides comprehensive protection.
Using anecdotal evidence or small sample sizes as though they constitute robust scientific data.
Stashed changes:docs/docs_dse/Biology/immunology.md
Misinterpreting graphs by confusing the independent and dependent variables or reading scales incorrectly.
which process is being described.
Stating that ‘enzymes are denatured by heat’ without specifying that high temperatures cause the change in tertiary structure.Stashed changes:docs/docs_dse/Biology/immunology.md
A[2_Immunology] --> B[Key Concepts]
A --> D[Practical Applications]
B --> E[Fundamental definitions]
D --> G[Real-world usage]
The key principles covered in this topic are linked in the sub-pages above. Focus on understanding the definitions, applying the formulas or frameworks, and evaluating strengths and limitations of each approach.
Worked examples demonstrating the application of key concepts are covered in the detailed sub-pages linked above.
